choriocarcinoma/hypoxia

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Mitochondrial Channel Opener Diazoxide Attenuates Hypoxia-Induced sFlt-1 Release in Human Choriocarcinoma Cells.

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OBJECTIVE To examine the effect of diazoxide on hypoxia-induced soluble fms-like tyrosin kinase-1 (sFlt-1) release in JEG-3 choriocarcinoma cells. METHODS Cells were cultured under normoxia (20% O2) or hypoxia (1% O2), and expression of sFlt-1 mRNA and protein release was determined by quantitative

Hypoxia downregulates continuous and interleukin-1-induced expression of human chorionic gonadotropin in choriocarcinoma cells.

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The effects of hypoxia on JEG-3, BeWo, and JAr cells were investigated and it was demonstrated that choriocarcinoma cells can be used as a model to study the molecular mechanism of hypoxia-mediated repression of human chorionic gonadotropin (hCG). Cells were maintained under hypoxia (3.5 per cent

Hypoxic upregulation of glucose transporters in BeWo choriocarcinoma cells is mediated by hypoxia-inducible factor-1.

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Placental hypoxia has been implicated in pregnancy pathologies, including fetal growth restriction and preeclampsia; however, the mechanism by which the trophoblast cell responds to hypoxia has not been adequately explored. Glucose transport, a process crucial to fetoplacental growth, is upregulated

Expression of placenta growth factor, soluble fms-like tyrosine kinase-1, metal-responsive transcription factor-1, heme oxygenase 1 and hypoxia inducible factor-1α mRNAs in pre-eclampsia placenta and the effect of pre-eclampsia sera on their expression of choriocarcinoma cells.

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OBJECTIVE We studied the effect of pre-eclampsia sera on the expression of placenta growth factor (PlGF), soluble fms-like tyrosine kinase-1 (sFlt-1), metal-responsive transcription factor-1 (MTF-1), heme oxygenase 1 (HO-1) and hypoxia inducible factor-1α (HIF-1α) mRNAs in JEG-3 cells

Expression of vascular endothelial growth factor (VEGF), hypoxia inducible factor 1 alpha (HIF-1alpha), and transforming growth factors beta1 (TGFbeta1) and beta3 (TGFbeta3) in gestational trophoblastic disease.

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The aim of this study was to investigate the relationship between the expression of vascular endothelial growth factor (VEGF), transforming growth factor beta (TGF-beta1 and TGF-beta3), and hypoxia inducible factor 1 alpha (HIF-1alpha) in gestational trophoblastic diseases to highlight the possible

Regulation of hypoxia-inducible factor-1α, regulated in development and DNA damage response-1 and mammalian target of rapamycin in human placental BeWo cells under hypoxia.

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Hypoxia-inducible factor-1 (HIF-1), regulated in development and DNA damage response-1 (REDD1) and mammalian target of rapamycin (mTOR) are crucial mediators of many metabolic processes in various cell types under hypoxia. The involvement and regulation of these three factors underlying

Hypoxia represses the differentiation of Rcho-1 rat trophoblast giant cells.

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BACKGROUND A hypoxic environment is known to be essential for early placentation. A low oxygen tension induces hypoxia-inducible factor-1 (HIF-1alpha) which may play an important role as a transcription factor in maintaining the proliferative and undifferentiated phenotype in human

Successful management of a patient with radiological presentation of choriocarcinoma syndrome before induction chemotherapy.

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Choriocarcinoma syndrome is a life-threatening lysis syndrome caused by blood vessel rupture and subsequent tumor bleeding. We describe a case of pretreatment choriocarcinoma syndrome that developed in a 27-year-old man. He underwent a high orchiectomy at a local hospital and was diagnosed with

Functional proteomics: examining the effects of hypoxia on the cytotrophoblast protein repertoire.

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The outcome of human pregnancy depends on the differentiation of cytotrophoblasts, specialized placental cells that physically connect the embryo/fetus to the mother. As cytotrophoblasts differentiate, they acquire tumor-like characteristics that enable them to invade the uterus. In a novel feedback

Regulation of the matricellular proteins CYR61 (CCN1) and NOV (CCN3) by hypoxia-inducible factor-1{alpha} and transforming-growth factor-{beta}3 in the human trophoblast.

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It is known that a hypoxic environment is critical for trophoblast migration and invasion and is fundamental for appropriate placental perfusion. Because cysteine-rich 61 (CYR61, CCN1) and nephroblastoma overexpressed (NOV, CCN3) are expressed in the extravillous trophoblast and expression levels

Metabolic Reprogramming of Trophoblast Cells in Response to Hypoxia.

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Hypoxia of trophoblast cells is an important regulator of normal development of the placenta. However, some pathological states associated with hypoxia, e.g. preeclampsia, impair the functions of placental cells. Oxyquinoline derivative inhibits HIF-prolyl hydroxylase by stabilizing HIF-1

Hypoxia-inducible factor 2 alpha impairs human cytotrophoblast syncytialization: New insights into placental dysfunction and fetal growth restriction

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Insufficient remodeling of uterine arteries causes pregnancy-related diseases, including fetal growth restriction and preeclampsia. In these situations, reduced maternal blood flow in the placenta is thought to be responsible for the persistence of a low oxygen environment throughout pregnancy. We

Effect of oxygen concentrations on sodium iodide symporter expression and iodide uptake and hCG expression in human choriocarcinoma BeWo cells.

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Normal human fetal development requires an adequate supply of thyroid hormone from conception. Until about 16 wk gestation this is supplied entirely by placental transfer of maternal hormone. Subsequently, the fetal thyroid synthesizes thyroid hormones, requiring a supply of maternal iodide.

Oxygen dependence of oestrogen production by human placental microsomes and cultured choriocarcinoma cells.

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The oxygen dependence of oestrogen (oestrone and 17 beta-oestradiol) formation from androstenedione and testosterone was studied in term human placental microsomes and in cultured human choriocarcinoma cells (BeWo line). Incubations were performed under various steady-state oxygen concentrations and

Expression of endothelial (type III) nitric oxide synthase in cytotrophoblastic cell lines: regulation by hypoxia and inflammatory cytokines.

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Expression of endothelial nitric oxide synthase (eNOS) has been localized to the villous syncytiotrophoblasts suggesting that NO release from these cells could prevent platelet adhesion and aggregation in the intervillous space. Hypoxia- or inflammation-dependent changes in the release of this

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